Endocrine Flashcards
another name for Somatropin?
GH
Somatropin MOA? AE?
MOA: synthetic growth hormone that has a role in bone, skeletal muscle and organ growth; increased red blood cell mass; transport of water, electrolytes and fluid and other functions
AE: fluid retention/edema, muscle and joint pain
Another name for Vasopressin?
antidiuretic hormone (ADH)
What do you give for bed wetting?
DDAVP
How to DDAVP work?
Increase permeability of water
PT concerns with Hypopituitarism
Drug treatment accuracy is difficult –> altered hormone levels exceeding normal ranges
Be alert for AE of elevated hormone levels
Low GH level = low bone density –> bone fractures, slipped capital femoral epiphyses
Ex of glucocorticoid
hydrocortisone, cortisol
Ex. Mineralocorticoid
Aldosterone
what is Addison disease?
insufficient production of cortisol and aldosterone
Cushing disease
Excessive glucocorticoids (exogenous or endogenous)
what can cause secondary adrenal insufficiency?
Taking glucocorticoids for a long time then stopped abruptly without tapering
What are short-term AE for glucocorticoids use?
↑ blood glucose, mood changes, fluid retention
What are long-term AE for glucorticoids use?
osteoporosis/↑fracture risk, thin skin, muscle wasting, poor wound healing, adrenal suppression, Cushing’s disease(to much steroid), ↑ risk of infection due to immunosuppression
Person with Glucocorticoid Deficiency- in times of stress or strenous exercise what should they do?
may require significantly higher med doses or require additional hydrocortisone before strenuous exercise
How do you treat Mineralocorticoid Excess/Hyperaldosteronism?
potassium sparing diuretic)
Spironolactone: nonselective for aldosterone receptors
Eplerenone: selective for aldosterone receptors-
What do you replace when someone has Glucocorticoid Deficiency and Mineralocorticoid Deficiency?
fludrocortisone
Therapeutic Concerns about Adrenal Steroids?
Catabolic effect on supporting tissues- Breakdown of muscle tissue, bone density 🡪 weakness, osteoporosis
Use caution to not overload muscles/bones during strengthening
Glucocorticoids and mineralocorticoids may cause HTN due to NA+ retaining properties
Immunosuppression: increased susceptibility to infection
How do you treat hypogonadism?
Testosterone replacement
What to look for in testosterone replacement?
weigh benefits of treating symptoms vs CV risk
No PO option due to hepatotoxicity
Topical placement varies by product but should always be covered by clothes
Risk with testosterone?
Possible ↑ risk of MI, stroke or CV death = only use if truly indicated
Prolonged use = ↑ risk hepatic toxicity (hepatitis, jaundice)
Anabolic-androgenic steroids
CV, cancer, infection, Endocrine: males- feminization; females- menstrual irregularities, Musculoskeletal: tendon/ligament rupture, Psych
Combination oral contraceptive AE?
↑ BP, N/V (usually improves after 2-3 cycles), weight gain, acne, depression
Rare: stroke, MI (especially if >35 years, uncontrolled HTN, smoker, DM)
Long-acting intrauterine device (IUD) risk
Monitor for device complications, copper associated with ↑ bleeding 🡪 anemia
Post-menopausal hormone replacement therapy (HRT)
treatment
Estrogen/progestogen combo or estrogen alone (if no uterus)
HRT risk
DVT, PE, breast cancer (with combo), endometrial cancer (with estrogen alone)
Therapeutic Concerns about Sex Hormones
Monitor blood pressure since these hormones promote Na+ and water retention (mineralocorticoid-like properties)
Negative effects: increased aggression, increased LDLs, gynecomastia
Other adverse effects: liver, cardiovascular, and reproductive abnormalities (reduce sperm count)
Hyperparathyroidism drug treatment
Calcimimetics and Bisphosphonates
Hypoparathyroidism drug treatment
calcium (1-3 grams per day) and vitamin D
Overtreatment may cause hypercalcemia and hypercalciuria (leading to nephrolithiasis/kidney stones)
Hashimoto’s disease symtoms
Hypothyroidism
Symptoms: bradycardia, anemia, lethargy, weight gain, cold intolerance, menstrual irregularities, generalized muscle weakness
Goiter may form from constant stimulation of TSH from lack of negative feedback
Levothyroxine (Synthroid) MOA, AE
MOA: convert T4 to T3
AE: typically well tolerated unless overtreat then will see symptoms of hyperthyroidism
Sweating, heat intolerance, tachycardia, diarrhea, nervousness, menstrual irregularities, ↑ basal metabolic rate
Levothyroxine (Synthroid) what to look out for
NTI drug- Requires monitoring and dose adjustments (initially every 4-8 weeks, then every 6-12 months when stable)
Take on empty stomach (30-60 minutes before AM meal, or 3-4 hours after PM meal, including coffee)
Separate from iron, calcium, magnesium, and aluminum containing products, or bile acid sequestrants by 4 hours due to binding thus not absorbed and make TSH levels go up
Overtreatment Levothyroxine (Synthroid)
Must monitor levels to avoid overtreatment
Refer to provider if symptoms of hyperthyroidism
If very excessive overdose can ↑ risk MI, HF, angina
Long-term overtreatment can lead to ↓ bone density and ↑ risk fractures
Due to osteoporosis, maintain lowest effective dose, especially in postmenopausal women
Graves Disease symtoms
Hyperthyroidism- thyroid storm can be fatal: dehydration, tachycardia, delirium, fever etc.
Goiter, exopthalmos (protruding eyes), high metabolism, nervousness, weight loss despite increased appetite
Graves disease drug treatment
Antithyroid meds- Methimazole
Methimazole MOA, AE
MOA: Blocks formation of T4and T3 by inhibiting oxidation of iodine
Common AE: rash, GI upset, arthralgia (refer to provider due to risk of rare but serious polyarthritis)
Treatment can cause hypothyroidism
What causes osteoporosis?
Occurs when formation of new bone does not keep up with bone resorption, due to a decline in osteoblast function
Medications for osteoperisis
Bisphosphonates (most common)
Denosumab
Sclerostin Inhibitor
Calcium and Vitamin D AE
Vitamin D dosage vary
GI- constipation
dosage will vary upon age
Bisphosphonates (-dronate) MOA, AE
MOA: binds to a key enzyme to inhibit the natural bone turnover pathways 🡪 ultimately ↑ osteoclast apoptosis which ↓ bone turnover
Most common AE: mild upper GI symptoms
Bisphosphonates (-dronate) what to look out for
Take with plain water 30-60 minutes before any food or medications and stay upright
Food and meds (especially proton-pump inhibitors; calcium, magnesium and iron such as MVI, antacids, supplements) can ↓ absorption up to 90%
GI AE are ↑ if not upright
Atypical femur fracture
monitoring with bisphosphonates
Other monitoring:
Hypocalcemia- refer to provider if muscle cramps/spasms, or numbness and tingling
Reports of severe joint, muscle and bone pain- refer back to provider
Denosumab (Prolia) MOA, AE
denosumab binds to RANKL which ultimately inhibits bone resorption
AE >10%: arthralgia,
atypical fracture, increase risk of infection
Sclerostin Inhibitors MOA AE
MOA: inhibits sclerostin, a regulatory factor in bone metabolism = ↑ bone formation
Most common AE: arthralgia
rare- atypical fractures
Therapeutic Concerns about Thyroid and Parathyroid drugs
Excessive doses of drugs used to treat either hyper- or hypofunction tend to produce symptoms of opposite disorder
Avoid overexertion in patients with decreased CO and hypotension caused by hypothyroidism
Excessive doses of calcium supplements for parathyroid dysfunction can alter cardiovascular function 🡪 arrhythmias
symptoms of hypoglycemia-
shakey, sweaty, dizzy, confused and difficulty speaking, hungry, weak or tired, hungry, nervous or upset
medication class to treat diabetes
Biguanide (metformin)
Sulfonylureas (SU)
Thiazolidinediones (TZD)
Dipeptidyl-peptidase 4 inhibitors (DPP-4i)
Sodium glucose co-transporter 2 inhibitors (SGLT2i)
Glucagon-like peptide 1 agonist (GLP1a)
Insulin
Metformin (Glucophage) MOA:
MOA: not fully known but inhibits production of glucose, inhibits intestinal absorption of glucose and increases insulin sensitivity in muscle and fat
Metformin (Glucophage) AE:
Common AE: GI (diarrhea, nausea, abdominal cramping/bloating)
Vitamin B12 deficiency: typically after extended look, can be misdiagnosed as peripheral neuropathy
glipizide- Class, MOA, AE, what to look out for
MOA: binds sulfonylurea receptor in the pancreas –> depolarization causes insulin release
AE: hypoglycemia (especially in elderly and renal dysfunction)
Typically before breakfast; immediate release must be 30 minutes before meal –> if not taken correctly may ↑ hypo risk
Thiazolidinedione (TZD)
MOA- “insulin sensitizer”
lowest hypoglycemia risk
Sitagliptin (Januvia) Class, MOA, AE
DPP-4 Inhibitors
increased incretin hormone levels → increase insulin synthesis/release and decrease glucagon secretion
low hypoglycemia risk
arthralgia
empagliflozin (Jardiance) Class, MOA, AE
SGLT2 inhibitor
MOA; blocks glucose reabsorption in the kidney thus ↑ urinary glucose excretion
Common AE: volume-depletion related AE (dehydration )
Some can reduce risk of renal complications, CV events
semaglutide (Ozempic)- Class, MOA, AE
other uses
GLP1 Receptor Agonist
↑ insulin secretion in presence of elevated glucose, ↓ glucagon secretion (which ↓ hepatic glucose production), slows gastric emptying (↑ satiety)
Common AE: GI (nausea, bloating, diarrhea)
obesity and CV events
Bolus rapid and regular onset/duration
Rapid:
Onset 10-30 minutes, duration 3-5+ hours
Regular (AKA: short)
Onset ~30 minutes, duration 4-12 hours
Typically inject before a meal (sometimes immediately after)
can also be used to correct hyperglycemia
therapeutic concerns with DM
> 300 mg/dL NO PHYSICAL THERAPY-
Below 100 mg/dL: eat a snack before activity
Monitor 6-12 hours after exercise
Know the symptoms of hypo- and hyperglycemia
Keep sugary drink/snack (orange juice, soda) readily available in case of hypoglycemia
Is the patient aware of hypo- or hyperglycemia symptoms?
Premeal insulin may need to be modified for postmeal exercise
Avoid heat/massage to area that was recently injected with insulin
Good footwear is critical!
